Document Detail

Effect of voluntary exercise on peripheral tissue glucocorticoid receptor content and the expression and activity of 11beta-HSD1 in the Syrian hamster.
MedLine Citation:
PMID:  16357069     Owner:  NLM     Status:  MEDLINE    
Recent findings indicate that elevated levels of glucocorticoids (GC), governed by the expression of 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1) and GC receptors (GR), in visceral adipose tissue and skeletal muscle lead to increased insulin resistance and the metabolic syndrome. Paradoxically, evidence indicates that aerobic exercise attenuates the development of the metabolic syndrome even though it stimulates acute increases in circulating GC levels. To investigate the hypothesis that training alters peripheral GC action to maintain insulin sensitivity, young male hamsters were randomly divided into sedentary (S) and trained (T) groups (n = 8 in each). The T group had 24-h access to running wheels over 4 wk of study. In muscle, T hamsters had lower 11beta-HSD1 protein expression (19.2 +/- 1.40 vs. 22.2 +/- 0.96 optical density, P < 0.05), similar 11beta-HSD1 enzyme activity (0.9 +/- 0.27% vs. 1.1 +/- 0.26), and lower GR protein expression (9.7 +/- 1.86 vs. 15.1 +/- 1.78 optical density, P < 0.01) than S hamsters. In liver, 11beta-HSD1 protein expression tended to be lower in T compared with S (19.2 +/- 0.56 vs. 21.4 +/- 1.05, P = 0.07), whereas both enzyme activity and GR protein expression were similar. In contrast, visceral adipose tissue contained approximately 2.7-fold higher 11beta-HSD1 enzyme activity in T compared with S (12.9 +/- 3.3 vs. 4.8 +/- 1.5% conversion, P < 0.05) but was considerably smaller in mass (0.24 +/- 0.02 vs. 0.71 +/- 0.06 g). Thus the intracellular adaptation of GC regulators to exercise is tissue specific, resulting in decreases in GC action in skeletal muscle and increases in GC action in visceral fat. These adaptations may have important implications in explaining the protective effects of aerobic exercise on insulin resistance and other symptoms of the metabolic syndrome.
Agnes E Coutinho; Jonathan E Campbell; Sergiu Fediuc; Michael C Riddell
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-12-15
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  100     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2006 May 
Date Detail:
Created Date:  2006-04-14     Completed Date:  2006-08-10     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1483-8     Citation Subset:  IM    
Department of Kinesiology and Health Science, York University, Toronto, Ontario, Canada.
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MeSH Terms
11-beta-Hydroxysteroid Dehydrogenases / biosynthesis,  physiology*
Adaptation, Physiological / physiology
Adipose Tissue / chemistry*,  physiology
Blood Glucose
Body Mass Index
Glucocorticoids / analysis,  blood,  physiology
Insulin Resistance / physiology
Intra-Abdominal Fat / chemistry,  physiology
Liver / chemistry,  physiology
Metabolic Syndrome X / etiology,  physiopathology
Muscle, Skeletal / chemistry*,  physiology
Physical Conditioning, Animal / physiology*
Random Allocation
Receptors, Glucocorticoid / biosynthesis,  physiology*
Reg. No./Substance:
0/Blood Glucose; 0/Glucocorticoids; 0/Insulin; 0/Receptors, Glucocorticoid; EC Dehydrogenases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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